Understanding the Cardiovascular System

Hi, welcome to Chapter 18, the cardiovascular system. So today we're going to identify the primary functions of blood, its fluid and cellular components and the physical characteristics. We're going to identify the most important proteins and the other solutes that are present in blood plasma, describe the formation of the formed elements component, sorry, the formed element components of blood, discuss the structure and function of those red blood cells and the hemoglobin, classify and characterize our white blood cells, describe the structure and the... platelets and explain the process of hemostasis, that's different than homeostasis, and explain the significance of our AB and RH blood groups and blood transfusions and discuss a variety of our blood disorders. So our cardiovascular system consists of three things. There's the pump. The pump obviously is the heart. There's the transport system. Those are going to be the blood vessels and then a fluid medium. And that's what we're going to talk about today is that fluid medium. So our blood is called the fluid medium. There's different components of blood, and remember that blood is, in fact, a connective tissue. Connective tissues have to have that extracellular matrix. So in the case of blood, plasma is considered that extracellular matrix, and it's unique because it is fluid. But there's also formed elements within the blood, and we call those formed elements because they are cells but also cell parts, like platelets or cell parts. So we have our red blood cells, also known as erythrocytes. We have our white blood cells, and then we have platelets. So what are the functions of blood? Big, big function is transportation. So we're going to be transporting oxygen, carbon dioxide, nutrients, metabolic waste, and hormones. There's also the function of blood as far as temperature regulation, immune defense, blood clotting. For our inflammatory response, for instance, we have that, and then white blood cells. So what does blood look like? Well, big thing about blood is that a lot of people think that deoxygenated blood is blue because they look at their veins and they appear blue, but that's not actually the case. Your blood is always red, but it does vary from a bright red to a dark red. Its temperature is about 38 degrees Celsius or is about 100.4 degrees Fahrenheit. The pH of blood averages at about 7.4, but we want it to stay between 7.35 and 7.45, and we use buffers in order to keep our blood pH. that narrow range. Our blood is approximately 8% of our adult body weight. So for males, that's typically about 5 to 6 liters. And for females, it's about 4 to 5 liters. So how does our blood volume affect our blood pressure? Typically, those that have a higher blood volume are going to have a higher blood pressure. So plasma is that fluid matrix, right? And it's about 92% water. There's also some things dissolved within that water. They're called plasma solutes, and so we have electrolytes. Electrolytes, you may also hear them referred to as ions or anions if they have a negative charge, or cations if they have a positive charge. And so in our blood plasma, we often see sodium, potassium, and calcium. We've talked about sodium, potassium, and calcium in prior units. We have dissolved gases like oxygen, carbon dioxide, and nitrogen. There's various organic nutrients here. This is where we're going to find some vitamins, lipids, glucose, amino acids, and our metabolic wastes, okay? So what does our blood look like? So in normal blood, this is actually called, we take what's called a hematocrit number, okay? And so that hematocrit number that we're looking at is the red blood cell content based in the blood, okay? So we put it into a centrifuge and it spins the blood. And then sort of those healthier elements are going to fall towards the bottom. And that is our hematocrit or our red blood cells. And so we see that we usually range between 37 and 52 percent of our hematocrit is considered normal. So in anemia, we have a depressed hematocrit. And then we can also have polycythemia, which is an elevated hematocrit. We also have in here our blood. We have what's called a buffy coat. And that buffy coat is going to be right in the center. And that is our white blood cells and platelets. That's usually about less than 1%. And then our blood plasma is anywhere between 47% and 62%. So what do we find within the plasma? We have a lot of plasma proteins. The big one that we're going to find is going to be albumin. Albumin is a major component of what we call osmotic pressure. And the osmotic pressure is sort of that pulling the water back toward it, right? That's osmosis. the movement of water. And so the water wants to move towards that albumin, so it causes an osmotic pressure of the plasma. We also have globulins, like antibodies. Antibodies are, in fact, called immunoglobulins. We also have transport proteins. We have fibrinogens. Fibrinogens help us to clot our blood. And then there are some other things like coagulation factors, which also help with blood clotting. Okay, so this is actually coming directly out of your textbook, so I encourage you to take a look at it. This is our component and our percent of blood, so the plasma is 46 to 63 percent here, right? And so what is our plasma really formed from? It's formed from water, plasma proteins, regular proteins, and then some other solutes. And you can see that we rather break it down over here, right? So our water is obviously fluid. Plasma proteins, we have albumin, globulins, fibrinogen. We have regulatory proteins like hormones and enzymes, and then we have nutrients, gases, and wastes. Where do we produce all of those things, and then what is the major function, right? So the water itself is really, it's the transport medium. Plasma proteins like albumin is for osmotic concentration, also helps us to transport lipid molecules. Albumin is also, it usually appears white, and that's because of the lipids contained within it. So lipids or fats are going to usually appear to be white, right? And then we have our globulins. So we have alpha globulins, beta globulins, and gamma globulins. The gamma globulins are going to be the immunoglobulins, which are going to be our antibodies, okay? So what are these formed elements? So we have the erythrocytes. Erythrocytes is a fancy word for red blood cells. Their big job is to carry the oxygen to our tissues and then carry some of our carbon dioxide to the lungs within the blood. And erythrocytes are essentially just a fancy bag. It's a carrying element, okay? Leukocytes are our white blood cells. They make up less than 1% of our blood. Their job is to fight infection. When we have been infected, we typically have a higher white blood cell count or a higher leukocyte count. And then we have platelets. And platelets are cell fragments. Those cell fragments are used for blood clotting, okay? And so you can see here, these are some of those formed elements. Like... Our leukocytes are our white blood cells. We have what I like to call the granfills. The granfills are granular leukocytes. And granular means that when we look under the microscope, we can see the grains within the cell itself. And so those granfills, as I like to call them, are the neutrophils, the eosinophils, and the basophils. We also have agranular leukocytes, meaning that we can't really see those granules when we look through the microscope. Those are lymphocytes and monocytes. Now, lymphocytes are going to be produced within the bone marrow and our lymphatic tissue. Monocytes are going to be in our red bone marrow. And really, you can see that their big job is immunity. Platelets is for hemostasis, which is blood clotting. So how do we get these formed elements? We do a process called hematopoiesis. That's a fun word to say. You should say that, hematopoiesis. Hematopoiesis occurs within the red bone marrow and it's found within cancellous bone. Remember, we have two different types of bone. We have cancellous bone and we have compact bone. So the compact bone is along sort of those edges of our long bones, right? It's that harder part, really compact and packed together, very densely packed cells. And then we have our cancellous bone or our spongy bone. We find that within the ends of our long bones, right? And so we do what's called extra medullary. hematopoiesis. That means that we're not going to do it within that bone marrow. So this is a different type of hematopoiesis. We could do that within the liver or the spleen, and we do that when the red marrow fails, meaning that it's not doing its job. All the formed elements are going to be sent directly into the bloodstream, except for a few of those white blood cells. White blood cells are called lymphocytes, some of them. They're going to head to the thymus for maturation and proliferation. Just some of them, those we call lymphocytes. T cells because thymus starts with T. The other ones we would call B cells because bone marrow starts with B. So here we can see that hematopoiesis sort of chart of how are we making these blood cells. So just most of the time you're always going to find that some of our cells are going to remain stem cells. So after division, some of them are going to remain stem cells. But the remaining stem cells are going to go on to two paths. We can go down the myeloid path on this side. or the lymphoid path over here. So the myeloid stem cells, they're going to give rise to what are called megakaryoblasts. Megakaryoblasts are going to eventually mature into megakaryocytes, which are then going to develop into platelets. Also, those myeloid stem cells can become proerythroblasts. Those proerythroblasts are going to become reticulocytes. And then eventually erythrocytes. Remember those erythrocytes? Those are red blood cells. We have myeloblasts. So those myeloblasts are going to go on to become our granfills, basophils, neutrophils, and eosinophils. And then we have the monoblasts are going to come on to become monocytes. Okay. So that's the myeloid side. We also have the lymphoid stem cell. This would be the other side of the family. Okay. These lymphoid stem cells are going to go on to become lymphoblasts, and then they can become either a natural killer cell or a small lymphocyte. Those small lymphocytes are going to be mature in two different areas. So we have the T lymphocytes that are going to mature within the thymus. and the B lymphocytes that are going to mature within the bone marrow. So how do we actually know to sort of drive and grow these? How do we know to do hematopoiesis, right? So we have two hormones. We have EPO and TPO. So erythropoietin, which is EPO, is secreted by the kidneys, and it does that in response to low oxygen levels. When we have low oxygen levels, it's like, oh, my gosh, we have low oxygen levels. we probably need more bags to carry the oxygen. We're not able to carry it all. So we're going to make some more red blood cells. That's EPO. And then we have TPO, which is thrombopoietin. Thrombopoietin is a hormone that's produced by our liver and our kidneys, and it helps to trigger our megakaryoblasts into megakaryocytes. Megakaryoblasts, megakaryocytes are going to become platelets. CPO, here we go. So it's secreted in here. It's going to go on to our megakaryocytes, and that can help us with increased platelet production. So you can see that whole process here. We also have what are called cholera-stimulating factors, or CSFs. These are cytokines. Cytokines are cell signals. They're produced by our red-blown marrow. leukocytes, macrophages, fibroblasts, and endothelial cells, and they trigger an increased production of our leukocytes or our white blood cells. Interleukins are another cytokine that we can do or we can release, and that's going to also increase our leukocyte production, right? So, CSFs and interleukins. So, our erythrocytes are, again, red blood cells, okay? These erythrocytes are going to differentiate from, to become these proerythrocytes. erythroblasts. Proerythroblasts are actually going to eventually eject out their nucleus, and then they become what are called reticulocytes. Those cell organelles are going to disappear, and then it leaves behind an erythrocyte. An erythrocyte is actually not a true cell. It's basically just a bag of hemoglobin for the purpose of transporting oxygen and carbon dioxide. It doesn't have the mitochondria in there. doesn't have mitochondria because if it did, it would use up the oxygen that it's carrying. Okay. And we obviously don't want it to use up that oxygen. We need it to carry the oxygen into the other cells so they can use it for cellular respiration, which you guys could see my hands moving right now. These erythrocytes, they have a biconcave shape that provides a greater surface area so that we can have more gas exchange happening relative to the volume. There's also this really special protein in there. It's called spectrin, and spectrin helps it to be flexible, and it helps it to squeeze through narrow capillaries. Hemoglobin inside of it is going to carry that oxygen, and that's actually what gives the red blood cells their red color. Hemoglobin is high in iron, and I don't know if you know a whole lot about rust, but when you put iron and you expose it to oxygen, it will rust, and rust has a red color to it. So your red blood cells are rust. nasty. So hemoglobin and oxygen transport. So hemoglobin is actually consists of heme and globin. Okay. And so globin is just four folded protein chains and they're designated as alpha one and alpha two, beta one and beta two. You can see them here. Here's the alpha one chain, the alpha two chain, the beta one and the beta two chain. Tucked inside of each one of them is that heme molecule and that heme molecule is where we're going to find that. iron. Each of the four iron molecules can bind to an oxygen molecule, and therefore, each hemoglobin molecule can transport four oxygen molecules. So, oxygen is required as that last step of the electron transport chain. If you remember cellular respiration, hopefully you remember cellular respiration. Glucose in the presence of oxygen is going to yield carbon dioxide and water as sort of our waste products, but... even more we're going to get a lot of energy or ATP out of that. And when we do cellular respiration in the presence of oxygen or aerobic respiration, we're going to use oxygen as that last step of that electron transport chain. And we need that oxygen in order to get the most energy out of the food that we eat. So the hemoglobin is going to carry that oxygen from the lungs to the tissues, and it does it as what's called oxyhemoglobin. So 98.5% of that oxygen is carried by that hemoglobin. 1.5% is dissolved within the plasma. When the oxygen is released, we call it deoxyhemoglobin. How do we transport carbon dioxide, though? So... Carbon dioxide can be carried within the red blood cells. It's called carb aminohemoglobin. That's about 20% of the carbon dioxide, okay? We also have this carbonic acid, okay? So carbonic acid gets dissolved in the plasma as carbonic acid. This is bicarbonate right here. And then carbon dioxide gets dissolved within the plasma as well. So how do we actually, we can actually recycle hemoglobin. Our body is really good at this. However, sometimes we don't do it so well. And when we don't do it so well, we actually get a buildup of bilirubin, which tends to have sort of a yellow tone to us, and it makes us appear jaundiced. So these are our red blood cells. And what happens is that those red blood cells are going to go through phagocytosis by a Kupfer cell. The Kupfer cells are most often found within the liver. They're going to break down that hemoglobin. into the heme and the globin. The globin itself can be further broken down into amino acids, and then we can use those to build different types of proteins. The heme, on the other hand, is going to get broken down into iron and bilirubin. The iron gets transported back to the bone marrow where it can make new red blood cells. The bilirubin, on the other hand, is going to be transported to the liver, and it's going to be broken down further into bile and then stored in the gallbladder for digestion. So sickle cell disease is when we have a single amino acid substitution within the hemoglobin molecule, and it results in what's called sickle hemoglobin or HGBS. Sickle hemoglobin is going to cause that erythrocyte to create a sickle shape. The sickle shape, we sometimes call it like a crescent moon shape. You can see it right here. You also see that it's not quite as red here, and that's because it's not really able to carry as much oxygen. because it doesn't have quite the same shape to it. But also, they're not flexible enough to squeeze through the capillaries. Capillaries are very, very tiny. It can get really, really tiny. And so these red blood cells that are hemoglobin or sickle hemoglobin, red blood cells are not going to be able to squeeze through those capillaries. They become wedged in place, and they can cause what's called sickle crises, because the tissues are going to become damaged due to a lack of oxygen. We can get joint damage or blindness may result. And it's more common in persons of African descent because it is genetic. There's different types of anemia. We have iron deficiency anemia. This has to do with a low dietary iron intake. It's really common among vegans, teens and toddlers that are more picky on their diet. And it prevents the heme synthesis. The red blood cells become small and pale. There's megaloblastic anemia. This is caused by a low dietary folate intake due to a lack of green leafy vegetables or rich cereals. It halts the red blood cell maturation, so they remain large and pale. There's pernicious anemia, which is a lack of vitamin B12. This can also halt that red blood cell maturation and can mimic the appearance of megaloblastic anemia. And then there's thalassemia, which is a missing or mutated genes for the alpha or the beta globins. This can cause anemia, and it is found in those of Mediterranean African descent. You can actually have both thalassemia and sickle cell anemia. So the classification of the leukocytes is that we divide those groups into different groups as to whether the cells contain those visible granules, like I've said. So we have those granular leukocytes, or the granfills. Those are from the myeloid series. We have the neutrophils. the eosinophils and the basophils right here. And then we have the agranular leukocytes, which are going to be the monocytes here from the myeloid stem cells. And then we also have the lymphocytes from the lymphoid series. So let's just review really quickly what phagocytosis is. Oftentimes we call phagocytosis sort of like cell eating. But really phagocytosis occurs when we're trying to get rid of something that can harm us. So like a bacteria, for instance. So we do what's called endocytosis or phagocytosis. We're going to be pulling in that bacteria and putting it within a lysosome. So we get a phagosome and then a lysosome. The lysosome and the phagosome are going to merge into one, and that's going to cause what we call a phagolysosome. The lysosomal enzymes are going to degrade the bacteria, and then we do what's called exocytosis to extrude out the waste, which is pus. Good times. These are those granular leukocytes, and you can sort of see how they look a little different from one another, but you can also see those granular pieces in here, right? So here's that neutrophil. The neutrophil is usually going to have three to five lobes to the nucleus, and it has sort of pale granules. And here is the eosinophil. They typically appear red under the microscope, so they have these red granules, and the basophils tend to appear blue. Okay, so these neutrophils, neutrophils make up about 50 to 70% of our total leukocyte count. Any higher count is going to indicate a bacterial infection. There's two to five lobes of those nucleus and we have these pale granules like lysosomes. We can do what's called respiratory burst. Respiratory burst is when we take hydrogen peroxide and bleach and they actually will burst and kill any intracellular pathogens and the cell. Defensins are pretty cool because they are proteins that can bind. two, and then they puncture any bacterial or fungal plasma membranes. They kind of like put a hole in it and then it just explodes. So their big defense is that they're going to do phagocysts of bacteria, right? So they're sort of non-specific immune defense. The eosinophils make up two to four percent of our total leukocyte count, but when we have a higher count, it can indicate a parasitic infection or even allergies. They have red granules within them. They have enzymes to help to destroy intestinal or even cutaneous or skin parasites. They also have antihistamine molecules. Antihistamine molecules are going to counteract histamine. Like we would take an antihistamine when we have an allergic response, like Benadryl, for instance, is an antihistamine. So our body actually releases histamine as an inflammatory response, but these eosinophils can actually release out an antihistamine to counteract them. And they are capable of phagocytosis, meaning that they can take in that parasite. These are basophils. Basophils tend to appear blue, those dark blue granules, to contain histamine for inflammation. And heparin, heparin is actually going to inhibit blood clotting. There are types of cells called mast cells. We haven't quite gotten to those yet. But I do want to tell you that they used to be thought to be tissue basophils. They're not. Mass cells actually reach maturity while in the tissues, but basophils are in the bone marrow. And so they're similar because they both arise from the same stem cells. So here's a monocyte and a lymphocyte. These are agranular leukocytes, meaning that we cannot see their granules. So monocytes make up 2% to 8% of our total leukocyte count, but a higher count can indicate that there's been a viral or a fungal infection. or even mononucleosis, hence the reason that we have mononucleosis. Maybe you've heard of mono before. It's like the kissing disease. It has a horseshoe-shaped nucleus. It's double the size of those granular leukocytes, but it does still have non-visible granules. We have cytokines in them. We have those defensives that can poke the holes and sort of cause bacteria, the fungi, to explode. And it has lysosomes, which are enzymes. So when we have these monocytes in tissues, we call them macrophages. So they're the same cells. They just are living in a different point. So they're not in the blood. They're found within the tissues, macrophages. Their big job is for surveillance. And they develop into antigen-presenting cells, meaning that they can alert other cells of an infection. And these macrophages are monocytes. Remember, macrophages are tissue, monocytes, and blood. They can, again, become what we call antigen-presenting cells. An antigen is something within or on a cell surface to say, sort of identify, right? And so we sometimes refer to it as like a flag, right? If I were to fly a flag, let's say, for the United States, then you would know that I'm an American, right? And so that kind of idea is to sort of identify you as to where you belong. And so each of my cells have, my name is Melissa, so I have a Melissa flag on them. And if there's a cell in my body that doesn't have the Melissa cell, then it alerts my leukocytes to start becoming activated. So what happens is that these macrophages can actually engulf a pathogen, engulf it into their phagosome. They remove the foreign flag or the antigen. from the pathogen. The pathogen is just something that can cause your infection. So for instance, a bacteria or a viral cell. Okay. So it places that foreign antigen on the cell surface and it attaches it to like a separate flagpole. That separate flagpole is called the MHC2 protein. Okay. Our self-flag or self-antigen are placed on the MHC1 proteins. Okay. So what happens is I engulfed that pathogen. It's tasted really good. Okay. I ate it up, but we know that we've been infected. And since we know we've been infected, I have to alert everyone else. So I take its flag off. I put it into my separate protein to say, hey, I'm still me on my MHC1. I'm good. This is me. But I have the flag or this antigen on my MHC2 flagpole. And I say, hey, we've been infected. So I carry that flag or that antigen flag that's on my MHC2 protein to my... CD4T lymphocytes that are found within my lymph nodes, okay? That's going to activate it, and it's going to find a specific B lymphocyte to start our adaptive immune response. We're going to go into way more details when we get to our lymphatic and immune system, okay? So we also have our A granular leukocytes, our lymphocytes. Lymphocytes make up 20 to 30 percent of our total leukocyte count. Higher count indicates that there's been a viral infection. So those that have been infected with, for instance, the coronavirus or COVID-19 would have a higher level of these lymphocytes. The nucleus is the entire cell and it has really small granular leukocytes. There's different types of T lymphocytes. There's the T lymphocytes that have matured in the thymus because thymus starts with the letter T. Its job is for cellular immune response. And then we have... B lymphocytes that mature in our bone marrow, and those are antibody production. So they're making antibodies. There's also memory cells. So we can have B cells or T cells that are going to form after exposure to the pathogen. Those help to mount a rapid response upon any subsequent exposures. They can live for years. This is one of the reasons that vaccines work. So these agranular leukocytes, like our CD4T lymphocytes, are also called T helper cells. They help to initiate an immune response and they bind to our MHC. MHC stands for major histocompatibility complex 1 and 2, which are found on our antipresenting cells. They trigger B cells to proliferate into plasma cells. Those plasma cells can then produce antibodies. Unfortunately, these types of cells are actually the ones that are killed by our human immunodeficiency virus or HIV. And when our counts of this particular leukocyte goes below 500, then we say that we've diagnosed with AIDS. Natural killer cells, our A cells, our CD8 lymphocytes, we can call them cytotoxic or natural killer cells. They recognize any cell that does not present itself and say, I'm you, I'm you, right? It doesn't have that normal cell flag. It's not holding the Melissa flag, so to speak. And so when that happens, it's going to go ahead and just kill it. It also can kill any cells that have bacteria or virus. And one of the ways that it does that is that it actually uses what are called perforins. Perforins are going to poke pores into any infected cell and cause it to burst open. And we have what are called granzymes. And granzymes are enzymes that enter through those pores and can cause the cell death. These are B lymphocytes. Those B lymphocytes can leave the bone marrow and they can then live within lymphoid follicles. Lymphoid follicles are found in the spleen, the lymph nodes, and the tonsils even. Remember, those CD4T lymphocytes are going to activate our B cell specific to the current infection. Those specific B cells are going to then proliferate as plasma cells, and the plasma cell is going to produce antibodies specific to the infection. Plasma cells and antibodies are mobilized within the bloodstream. So remember, we have these B lymphocytes. B lymphocytes, once they've been activated by a T lymphocyte, okay, B cells are activated by a specific T lymphocyte, okay, it's going to cause that B cell to sort of start to make new plasma cells. And those new plasma cells are producing an antibody that's specific to that infection, right? So let's pretend that. I have come into contact with a virus. That virus has infected one of my cells. That virus had a specific antigen flag. on the cell that said, oh, not myself. Since that's the case, my CD40 lymphocyte said, oh, no, you're not good. You're not good. I'm going to activate the specific B cells. Those B cells are going to copy themselves into new plasma cells. Those plasma cells are going to produce antibodies that are supposed to that virus. And antibodies are pretty cool because their big job is to sort of like clump around a cell. and it won't allow it to attach to anything else. Let's talk about hemostasis. Hemostasis is blood clotting. And the way that we do sort of form a blood clot is first we have to have an injury. So a blood vessel is going to be severed. Remember, we have all these white blood cells and red blood cells or erythrocytes and platelets in our blood all the time, right? So they're starting to leak out. When that happens, we get what's called a vascular spasm. So the smooth muscle within that vessel wall is going to contract, and that helps to reduce any blood loss. Now remember that we're sending platelets through kind of all the time. They're all found within our blood. But the platelets have to be activated. And so those are going to be activated by some chemicals or some cytokines that are released from the injury site. and by contact with underlying collagen. Remember, we have collagen within the vessel walls. So once it's been broken, it's going to become activated. So these platelets are going to be activated by those chemical signals. Then those, remember, this is a positive feedback mechanism. So those platelets are then going to send out more signals and more signals. And we're going to form what we call a platelet plug. Okay. Then we're going to have coagulation. So. Coagulation means that we have what are called fibrinogen. Remember, fibrinogen is going to make fibrin. That fibrinogen is going to be converted over to fibrin, and that's going to form sort of a mesh net, and that mesh net is going to trap more platelets and more erythrocytes, and that's going to form an actual clot, and that's called coagulation. There's different types of blood types. So we have ABO blood types. So type A, we can have... AA or AO. We can have type B, B, BO. Whoops. We can have type AB. We can have type O. Okay. So when we look here, here's type A blood. Okay. So this is our red blood cell surface. It has all of these fun flags out here saying, hi, I'm in type A. Okay. And look, it also, we have antibodies to Bs. Okay. Here's type B. So this is the B flag saying, hi, I'm a B cell. And then we have plasma antibodies of A. Okay. So that means that people with type B cannot receive a transfusion with type A blood, just like those who have type A cannot receive type B blood. Okay. So type AB, you can see they have a flag that says we're A and B. but we don't have any plasma antibodies. Type O doesn't have any flag on it, okay? But it does have antibodies to both A and B. So what does that mean exactly? Okay, these are the donor blood types and these are the recipient blood types, okay? AB positive, they are looking really good because they are called the universal recipient, meaning that they can receive blood from any donor. O negative, on the other hand, poor guys, they can only get blood from other O negatives, okay? So where do we have that positive and negative come through, right? So we have what's called the Rh blood group. This is identified by the presence or the absence of what's called an RhD antigen, okay? So we're either Rh negative or Rh positive, okay? So this is Rh positive. This is Rh negative. meaning that we don't have it. 85% of Americans are Rh positive. This is distinct from our ABO blood types. So unlike our ABO groups with our preformed antibodies, an Rh negative individual only develops antibodies if exposed to the Rh antigen. And that would be deadly when an Rh negative mother is pregnant with an Rh positive baby. So how does this happen exactly? So during birth, Okay, this is our first exposure, so the birth of the first Rh-positive infant. Okay, so this first infant, totally fine. Okay, during birth, the Rh-positive fetal erythrocytes are going to leak into the maternal blood. That's because we've broken off the embryonic chorion, and that normally isolates the fetal and maternal blood. But during birth, it's broken. The maternal B cells would be activated by the Rh antigen that was present within the fetal or the baby. And that produces large amounts of anti-Rh antibodies. Now, in any next birth, now the Rh antibody within the mother's blood is elevated after that first exposure that happened. So now the Rh antibodies are actually small enough to cross the embryonic chorion, and it can attack any fetal erythrocytes. So what I'd like you to do is take a second and fill in this chart, and that is one of your assignments. If you have any questions, please feel free to reach out to me. I am here to answer them.

So our cardiovascular system consists of three things. There's the pump. The pump obviously is the heart.

There's the transport system. Those are going to be the blood vessels and then a fluid medium. And that's what we're going to talk about today is that fluid medium.

So our blood is called the fluid medium. There's different components of blood, and remember that blood is, in fact, a connective tissue. Connective tissues have to have that extracellular matrix.

So in the case of blood, plasma is considered that extracellular matrix, and it's unique because it is fluid. But there's also formed elements within the blood, and we call those formed elements because they are cells but also cell parts, like platelets or cell parts. So we have our red blood cells, also known as erythrocytes.

We have our white blood cells, and then we have platelets. So what are the functions of blood? Big, big function is transportation. So we're going to be transporting oxygen, carbon dioxide, nutrients, metabolic waste, and hormones. There's also the function of blood as far as temperature regulation, immune defense, blood clotting.

For our inflammatory response, for instance, we have that, and then white blood cells. So what does blood look like? Well, big thing about blood is that a lot of people think that deoxygenated blood is blue because they look at their veins and they appear blue, but that's not actually the case.

Your blood is always red, but it does vary from a bright red to a dark red. Its temperature is about 38 degrees Celsius or is about 100.4 degrees Fahrenheit. The pH of blood averages at about 7.4, but we want it to stay between 7.35 and 7.45, and we use buffers in order to keep our blood pH. that narrow range. Our blood is approximately 8% of our adult body weight. So for males, that's typically about 5 to 6 liters.

And for females, it's about 4 to 5 liters. So how does our blood volume affect our blood pressure? Typically, those that have a higher blood volume are going to have a higher blood pressure.

So plasma is that fluid matrix, right? And it's about 92% water. There's also some things dissolved within that water.

They're called plasma solutes, and so we have electrolytes. Electrolytes, you may also hear them referred to as ions or anions if they have a negative charge, or cations if they have a positive charge. And so in our blood plasma, we often see sodium, potassium, and calcium. We've talked about sodium, potassium, and calcium in prior units. We have dissolved gases like oxygen, carbon dioxide, and nitrogen.

There's various organic nutrients here. This is where we're going to find some vitamins, lipids, glucose, amino acids, and our metabolic wastes, okay? So what does our blood look like? So in normal blood, this is actually called, we take what's called a hematocrit number, okay? And so that hematocrit number that we're looking at is the red blood cell content based in the blood, okay?

So we put it into a centrifuge and it spins the blood. And then sort of those healthier elements are going to fall towards the bottom. And that is our hematocrit or our red blood cells.

And so we see that we usually range between 37 and 52 percent of our hematocrit is considered normal. So in anemia, we have a depressed hematocrit. And then we can also have polycythemia, which is an elevated hematocrit.

We also have in here our blood. We have what's called a buffy coat. And that buffy coat is going to be right in the center.

And that is our white blood cells and platelets. That's usually about less than 1%. And then our blood plasma is anywhere between 47% and 62%.

So what do we find within the plasma? We have a lot of plasma proteins. The big one that we're going to find is going to be albumin.

Albumin is a major component of what we call osmotic pressure. And the osmotic pressure is sort of that pulling the water back toward it, right? That's osmosis. the movement of water.

And so the water wants to move towards that albumin, so it causes an osmotic pressure of the plasma. We also have globulins, like antibodies. Antibodies are, in fact, called immunoglobulins. We also have transport proteins. We have fibrinogens.

Fibrinogens help us to clot our blood. And then there are some other things like coagulation factors, which also help with blood clotting. Okay, so this is actually coming directly out of your textbook, so I encourage you to take a look at it.

This is our component and our percent of blood, so the plasma is 46 to 63 percent here, right? And so what is our plasma really formed from? It's formed from water, plasma proteins, regular proteins, and then some other solutes.

And you can see that we rather break it down over here, right? So our water is obviously fluid. Plasma proteins, we have albumin, globulins, fibrinogen. We have regulatory proteins like hormones and enzymes, and then we have nutrients, gases, and wastes.

Where do we produce all of those things, and then what is the major function, right? So the water itself is really, it's the transport medium. Plasma proteins like albumin is for osmotic concentration, also helps us to transport lipid molecules. Albumin is also, it usually appears white, and that's because of the lipids contained within it.

So lipids or fats are going to usually appear to be white, right? And then we have our globulins. So we have alpha globulins, beta globulins, and gamma globulins.

The gamma globulins are going to be the immunoglobulins, which are going to be our antibodies, okay? So what are these formed elements? So we have the erythrocytes. Erythrocytes is a fancy word for red blood cells.

Their big job is to carry the oxygen to our tissues and then carry some of our carbon dioxide to the lungs within the blood. And erythrocytes are essentially just a fancy bag. It's a carrying element, okay?

Leukocytes are our white blood cells. They make up less than 1% of our blood. Their job is to fight infection. When we have been infected, we typically have a higher white blood cell count or a higher leukocyte count. And then we have platelets.

And platelets are cell fragments. Those cell fragments are used for blood clotting, okay? And so you can see here, these are some of those formed elements. Like... Our leukocytes are our white blood cells.

We have what I like to call the granfills. The granfills are granular leukocytes. And granular means that when we look under the microscope, we can see the grains within the cell itself. And so those granfills, as I like to call them, are the neutrophils, the eosinophils, and the basophils.

We also have agranular leukocytes, meaning that we can't really see those granules when we look through the microscope. Those are lymphocytes and monocytes. Now, lymphocytes are going to be produced within the bone marrow and our lymphatic tissue. Monocytes are going to be in our red bone marrow. And really, you can see that their big job is immunity.

Platelets is for hemostasis, which is blood clotting. So how do we get these formed elements? We do a process called hematopoiesis.

That's a fun word to say. You should say that, hematopoiesis. Hematopoiesis occurs within the red bone marrow and it's found within cancellous bone.

Remember, we have two different types of bone. We have cancellous bone and we have compact bone. So the compact bone is along sort of those edges of our long bones, right? It's that harder part, really compact and packed together, very densely packed cells.

And then we have our cancellous bone or our spongy bone. We find that within the ends of our long bones, right? And so we do what's called extra medullary.

hematopoiesis. That means that we're not going to do it within that bone marrow. So this is a different type of hematopoiesis. We could do that within the liver or the spleen, and we do that when the red marrow fails, meaning that it's not doing its job. All the formed elements are going to be sent directly into the bloodstream, except for a few of those white blood cells.

White blood cells are called lymphocytes, some of them. They're going to head to the thymus for maturation and proliferation. Just some of them, those we call lymphocytes. T cells because thymus starts with T.

The other ones we would call B cells because bone marrow starts with B. So here we can see that hematopoiesis sort of chart of how are we making these blood cells. So just most of the time you're always going to find that some of our cells are going to remain stem cells.

So after division, some of them are going to remain stem cells. But the remaining stem cells are going to go on to two paths. We can go down the myeloid path on this side. or the lymphoid path over here. So the myeloid stem cells, they're going to give rise to what are called megakaryoblasts.

Megakaryoblasts are going to eventually mature into megakaryocytes, which are then going to develop into platelets. Also, those myeloid stem cells can become proerythroblasts. Those proerythroblasts are going to become reticulocytes.

And then eventually erythrocytes. Remember those erythrocytes? Those are red blood cells. We have myeloblasts. So those myeloblasts are going to go on to become our granfills, basophils, neutrophils, and eosinophils.

And then we have the monoblasts are going to come on to become monocytes. Okay. So that's the myeloid side.

We also have the lymphoid stem cell. This would be the other side of the family. Okay.

These lymphoid stem cells are going to go on to become lymphoblasts, and then they can become either a natural killer cell or a small lymphocyte. Those small lymphocytes are going to be mature in two different areas. So we have the T lymphocytes that are going to mature within the thymus. and the B lymphocytes that are going to mature within the bone marrow. So how do we actually know to sort of drive and grow these?

How do we know to do hematopoiesis, right? So we have two hormones. We have EPO and TPO.

So erythropoietin, which is EPO, is secreted by the kidneys, and it does that in response to low oxygen levels. When we have low oxygen levels, it's like, oh, my gosh, we have low oxygen levels. we probably need more bags to carry the oxygen.

We're not able to carry it all. So we're going to make some more red blood cells. That's EPO.

And then we have TPO, which is thrombopoietin. Thrombopoietin is a hormone that's produced by our liver and our kidneys, and it helps to trigger our megakaryoblasts into megakaryocytes. Megakaryoblasts, megakaryocytes are going to become platelets. CPO, here we go.

So it's secreted in here. It's going to go on to our megakaryocytes, and that can help us with increased platelet production. So you can see that whole process here.

We also have what are called cholera-stimulating factors, or CSFs. These are cytokines. Cytokines are cell signals. They're produced by our red-blown marrow.

leukocytes, macrophages, fibroblasts, and endothelial cells, and they trigger an increased production of our leukocytes or our white blood cells. Interleukins are another cytokine that we can do or we can release, and that's going to also increase our leukocyte production, right? So, CSFs and interleukins. So, our erythrocytes are, again, red blood cells, okay?

These erythrocytes are going to differentiate from, to become these proerythrocytes. erythroblasts. Proerythroblasts are actually going to eventually eject out their nucleus, and then they become what are called reticulocytes.

Those cell organelles are going to disappear, and then it leaves behind an erythrocyte. An erythrocyte is actually not a true cell. It's basically just a bag of hemoglobin for the purpose of transporting oxygen and carbon dioxide. It doesn't have the mitochondria in there. doesn't have mitochondria because if it did, it would use up the oxygen that it's carrying.

Okay. And we obviously don't want it to use up that oxygen. We need it to carry the oxygen into the other cells so they can use it for cellular respiration, which you guys could see my hands moving right now.

These erythrocytes, they have a biconcave shape that provides a greater surface area so that we can have more gas exchange happening relative to the volume. There's also this really special protein in there. It's called spectrin, and spectrin helps it to be flexible, and it helps it to squeeze through narrow capillaries. Hemoglobin inside of it is going to carry that oxygen, and that's actually what gives the red blood cells their red color. Hemoglobin is high in iron, and I don't know if you know a whole lot about rust, but when you put iron and you expose it to oxygen, it will rust, and rust has a red color to it.

So your red blood cells are rust. nasty. So hemoglobin and oxygen transport. So hemoglobin is actually consists of heme and globin. Okay.

And so globin is just four folded protein chains and they're designated as alpha one and alpha two, beta one and beta two. You can see them here. Here's the alpha one chain, the alpha two chain, the beta one and the beta two chain.

Tucked inside of each one of them is that heme molecule and that heme molecule is where we're going to find that. iron. Each of the four iron molecules can bind to an oxygen molecule, and therefore, each hemoglobin molecule can transport four oxygen molecules. So, oxygen is required as that last step of the electron transport chain.

If you remember cellular respiration, hopefully you remember cellular respiration. Glucose in the presence of oxygen is going to yield carbon dioxide and water as sort of our waste products, but... even more we're going to get a lot of energy or ATP out of that. And when we do cellular respiration in the presence of oxygen or aerobic respiration, we're going to use oxygen as that last step of that electron transport chain. And we need that oxygen in order to get the most energy out of the food that we eat.

So the hemoglobin is going to carry that oxygen from the lungs to the tissues, and it does it as what's called oxyhemoglobin. So 98.5% of that oxygen is carried by that hemoglobin. 1.5% is dissolved within the plasma. When the oxygen is released, we call it deoxyhemoglobin.

How do we transport carbon dioxide, though? So... Carbon dioxide can be carried within the red blood cells.

It's called carb aminohemoglobin. That's about 20% of the carbon dioxide, okay? We also have this carbonic acid, okay?

So carbonic acid gets dissolved in the plasma as carbonic acid. This is bicarbonate right here. And then carbon dioxide gets dissolved within the plasma as well.

So how do we actually, we can actually recycle hemoglobin. Our body is really good at this. However, sometimes we don't do it so well. And when we don't do it so well, we actually get a buildup of bilirubin, which tends to have sort of a yellow tone to us, and it makes us appear jaundiced. So these are our red blood cells.

And what happens is that those red blood cells are going to go through phagocytosis by a Kupfer cell. The Kupfer cells are most often found within the liver. They're going to break down that hemoglobin. into the heme and the globin.

The globin itself can be further broken down into amino acids, and then we can use those to build different types of proteins. The heme, on the other hand, is going to get broken down into iron and bilirubin. The iron gets transported back to the bone marrow where it can make new red blood cells.

The bilirubin, on the other hand, is going to be transported to the liver, and it's going to be broken down further into bile and then stored in the gallbladder for digestion. So sickle cell disease is when we have a single amino acid substitution within the hemoglobin molecule, and it results in what's called sickle hemoglobin or HGBS. Sickle hemoglobin is going to cause that erythrocyte to create a sickle shape. The sickle shape, we sometimes call it like a crescent moon shape.

You can see it right here. You also see that it's not quite as red here, and that's because it's not really able to carry as much oxygen. because it doesn't have quite the same shape to it. But also, they're not flexible enough to squeeze through the capillaries. Capillaries are very, very tiny.

It can get really, really tiny. And so these red blood cells that are hemoglobin or sickle hemoglobin, red blood cells are not going to be able to squeeze through those capillaries. They become wedged in place, and they can cause what's called sickle crises, because the tissues are going to become damaged due to a lack of oxygen. We can get joint damage or blindness may result. And it's more common in persons of African descent because it is genetic.

There's different types of anemia. We have iron deficiency anemia. This has to do with a low dietary iron intake.

It's really common among vegans, teens and toddlers that are more picky on their diet. And it prevents the heme synthesis. The red blood cells become small and pale. There's megaloblastic anemia. This is caused by a low dietary folate intake due to a lack of green leafy vegetables or rich cereals.

It halts the red blood cell maturation, so they remain large and pale. There's pernicious anemia, which is a lack of vitamin B12. This can also halt that red blood cell maturation and can mimic the appearance of megaloblastic anemia.

And then there's thalassemia, which is a missing or mutated genes for the alpha or the beta globins. This can cause anemia, and it is found in those of Mediterranean African descent. You can actually have both thalassemia and sickle cell anemia.

So the classification of the leukocytes is that we divide those groups into different groups as to whether the cells contain those visible granules, like I've said. So we have those granular leukocytes, or the granfills. Those are from the myeloid series.

We have the neutrophils. the eosinophils and the basophils right here. And then we have the agranular leukocytes, which are going to be the monocytes here from the myeloid stem cells. And then we also have the lymphocytes from the lymphoid series.

So let's just review really quickly what phagocytosis is. Oftentimes we call phagocytosis sort of like cell eating. But really phagocytosis occurs when we're trying to get rid of something that can harm us.

So like a bacteria, for instance. So we do what's called endocytosis or phagocytosis. We're going to be pulling in that bacteria and putting it within a lysosome.

So we get a phagosome and then a lysosome. The lysosome and the phagosome are going to merge into one, and that's going to cause what we call a phagolysosome. The lysosomal enzymes are going to degrade the bacteria, and then we do what's called exocytosis to extrude out the waste, which is pus. Good times. These are those granular leukocytes, and you can sort of see how they look a little different from one another, but you can also see those granular pieces in here, right?

So here's that neutrophil. The neutrophil is usually going to have three to five lobes to the nucleus, and it has sort of pale granules. And here is the eosinophil.

They typically appear red under the microscope, so they have these red granules, and the basophils tend to appear blue. Okay, so these neutrophils, neutrophils make up about 50 to 70% of our total leukocyte count. Any higher count is going to indicate a bacterial infection. There's two to five lobes of those nucleus and we have these pale granules like lysosomes.

We can do what's called respiratory burst. Respiratory burst is when we take hydrogen peroxide and bleach and they actually will burst and kill any intracellular pathogens and the cell. Defensins are pretty cool because they are proteins that can bind.

two, and then they puncture any bacterial or fungal plasma membranes. They kind of like put a hole in it and then it just explodes. So their big defense is that they're going to do phagocysts of bacteria, right? So they're sort of non-specific immune defense. The eosinophils make up two to four percent of our total leukocyte count, but when we have a higher count, it can indicate a parasitic infection or even allergies.

They have red granules within them. They have enzymes to help to destroy intestinal or even cutaneous or skin parasites. They also have antihistamine molecules.

Antihistamine molecules are going to counteract histamine. Like we would take an antihistamine when we have an allergic response, like Benadryl, for instance, is an antihistamine. So our body actually releases histamine as an inflammatory response, but these eosinophils can actually release out an antihistamine to counteract them.

And they are capable of phagocytosis, meaning that they can take in that parasite. These are basophils. Basophils tend to appear blue, those dark blue granules, to contain histamine for inflammation. And heparin, heparin is actually going to inhibit blood clotting. There are types of cells called mast cells.

We haven't quite gotten to those yet. But I do want to tell you that they used to be thought to be tissue basophils. They're not. Mass cells actually reach maturity while in the tissues, but basophils are in the bone marrow.

And so they're similar because they both arise from the same stem cells. So here's a monocyte and a lymphocyte. These are agranular leukocytes, meaning that we cannot see their granules. So monocytes make up 2% to 8% of our total leukocyte count, but a higher count can indicate that there's been a viral or a fungal infection. or even mononucleosis, hence the reason that we have mononucleosis.

Maybe you've heard of mono before. It's like the kissing disease. It has a horseshoe-shaped nucleus. It's double the size of those granular leukocytes, but it does still have non-visible granules.

We have cytokines in them. We have those defensives that can poke the holes and sort of cause bacteria, the fungi, to explode. And it has lysosomes, which are enzymes. So when we have these monocytes in tissues, we call them macrophages. So they're the same cells.

They just are living in a different point. So they're not in the blood. They're found within the tissues, macrophages. Their big job is for surveillance.

And they develop into antigen-presenting cells, meaning that they can alert other cells of an infection. And these macrophages are monocytes. Remember, macrophages are tissue, monocytes, and blood.

They can, again, become what we call antigen-presenting cells. An antigen is something within or on a cell surface to say, sort of identify, right? And so we sometimes refer to it as like a flag, right?

If I were to fly a flag, let's say, for the United States, then you would know that I'm an American, right? And so that kind of idea is to sort of identify you as to where you belong. And so each of my cells have, my name is Melissa, so I have a Melissa flag on them. And if there's a cell in my body that doesn't have the Melissa cell, then it alerts my leukocytes to start becoming activated.

So what happens is that these macrophages can actually engulf a pathogen, engulf it into their phagosome. They remove the foreign flag or the antigen. from the pathogen. The pathogen is just something that can cause your infection.

So for instance, a bacteria or a viral cell. Okay. So it places that foreign antigen on the cell surface and it attaches it to like a separate flagpole.

That separate flagpole is called the MHC2 protein. Okay. Our self-flag or self-antigen are placed on the MHC1 proteins.

Okay. So what happens is I engulfed that pathogen. It's tasted really good.

Okay. I ate it up, but we know that we've been infected. And since we know we've been infected, I have to alert everyone else. So I take its flag off.

I put it into my separate protein to say, hey, I'm still me on my MHC1. I'm good. This is me.

But I have the flag or this antigen on my MHC2 flagpole. And I say, hey, we've been infected. So I carry that flag or that antigen flag that's on my MHC2 protein to my...

CD4T lymphocytes that are found within my lymph nodes, okay? That's going to activate it, and it's going to find a specific B lymphocyte to start our adaptive immune response. We're going to go into way more details when we get to our lymphatic and immune system, okay?

So we also have our A granular leukocytes, our lymphocytes. Lymphocytes make up 20 to 30 percent of our total leukocyte count. Higher count indicates that there's been a viral infection.

So those that have been infected with, for instance, the coronavirus or COVID-19 would have a higher level of these lymphocytes. The nucleus is the entire cell and it has really small granular leukocytes. There's different types of T lymphocytes. There's the T lymphocytes that have matured in the thymus because thymus starts with the letter T. Its job is for cellular immune response.

And then we have... B lymphocytes that mature in our bone marrow, and those are antibody production. So they're making antibodies.

There's also memory cells. So we can have B cells or T cells that are going to form after exposure to the pathogen. Those help to mount a rapid response upon any subsequent exposures.

They can live for years. This is one of the reasons that vaccines work. So these agranular leukocytes, like our CD4T lymphocytes, are also called T helper cells. They help to initiate an immune response and they bind to our MHC. MHC stands for major histocompatibility complex 1 and 2, which are found on our antipresenting cells.

They trigger B cells to proliferate into plasma cells. Those plasma cells can then produce antibodies. Unfortunately, these types of cells are actually the ones that are killed by our human immunodeficiency virus or HIV.

And when our counts of this particular leukocyte goes below 500, then we say that we've diagnosed with AIDS. Natural killer cells, our A cells, our CD8 lymphocytes, we can call them cytotoxic or natural killer cells. They recognize any cell that does not present itself and say, I'm you, I'm you, right?

It doesn't have that normal cell flag. It's not holding the Melissa flag, so to speak. And so when that happens, it's going to go ahead and just kill it.

It also can kill any cells that have bacteria or virus. And one of the ways that it does that is that it actually uses what are called perforins. Perforins are going to poke pores into any infected cell and cause it to burst open. And we have what are called granzymes. And granzymes are enzymes that enter through those pores and can cause the cell death.

These are B lymphocytes. Those B lymphocytes can leave the bone marrow and they can then live within lymphoid follicles. Lymphoid follicles are found in the spleen, the lymph nodes, and the tonsils even. Remember, those CD4T lymphocytes are going to activate our B cell specific to the current infection.

Those specific B cells are going to then proliferate as plasma cells, and the plasma cell is going to produce antibodies specific to the infection. Plasma cells and antibodies are mobilized within the bloodstream. So remember, we have these B lymphocytes. B lymphocytes, once they've been activated by a T lymphocyte, okay, B cells are activated by a specific T lymphocyte, okay, it's going to cause that B cell to sort of start to make new plasma cells. And those new plasma cells are producing an antibody that's specific to that infection, right?

So let's pretend that. I have come into contact with a virus. That virus has infected one of my cells.

That virus had a specific antigen flag. on the cell that said, oh, not myself. Since that's the case, my CD40 lymphocyte said, oh, no, you're not good.

You're not good. I'm going to activate the specific B cells. Those B cells are going to copy themselves into new plasma cells. Those plasma cells are going to produce antibodies that are supposed to that virus. And antibodies are pretty cool because their big job is to sort of like clump around a cell.

and it won't allow it to attach to anything else. Let's talk about hemostasis. Hemostasis is blood clotting.

And the way that we do sort of form a blood clot is first we have to have an injury. So a blood vessel is going to be severed. Remember, we have all these white blood cells and red blood cells or erythrocytes and platelets in our blood all the time, right? So they're starting to leak out. When that happens, we get what's called a vascular spasm.

So the smooth muscle within that vessel wall is going to contract, and that helps to reduce any blood loss. Now remember that we're sending platelets through kind of all the time. They're all found within our blood.

But the platelets have to be activated. And so those are going to be activated by some chemicals or some cytokines that are released from the injury site. and by contact with underlying collagen. Remember, we have collagen within the vessel walls. So once it's been broken, it's going to become activated.

So these platelets are going to be activated by those chemical signals. Then those, remember, this is a positive feedback mechanism. So those platelets are then going to send out more signals and more signals.

And we're going to form what we call a platelet plug. Okay. Then we're going to have coagulation.

So. Coagulation means that we have what are called fibrinogen. Remember, fibrinogen is going to make fibrin.

That fibrinogen is going to be converted over to fibrin, and that's going to form sort of a mesh net, and that mesh net is going to trap more platelets and more erythrocytes, and that's going to form an actual clot, and that's called coagulation. There's different types of blood types. So we have ABO blood types. So type A, we can have... AA or AO.

We can have type B, B, BO. Whoops. We can have type AB.

We can have type O. Okay. So when we look here, here's type A blood.

Okay. So this is our red blood cell surface. It has all of these fun flags out here saying, hi, I'm in type A. Okay. And look, it also, we have antibodies to Bs.

Okay. Here's type B. So this is the B flag saying, hi, I'm a B cell. And then we have plasma antibodies of A.

Okay. So that means that people with type B cannot receive a transfusion with type A blood, just like those who have type A cannot receive type B blood. Okay.

So type AB, you can see they have a flag that says we're A and B. but we don't have any plasma antibodies. Type O doesn't have any flag on it, okay? But it does have antibodies to both A and B.

So what does that mean exactly? Okay, these are the donor blood types and these are the recipient blood types, okay? AB positive, they are looking really good because they are called the universal recipient, meaning that they can receive blood from any donor.

O negative, on the other hand, poor guys, they can only get blood from other O negatives, okay? So where do we have that positive and negative come through, right? So we have what's called the Rh blood group. This is identified by the presence or the absence of what's called an RhD antigen, okay?

So we're either Rh negative or Rh positive, okay? So this is Rh positive. This is Rh negative. meaning that we don't have it. 85% of Americans are Rh positive.

This is distinct from our ABO blood types. So unlike our ABO groups with our preformed antibodies, an Rh negative individual only develops antibodies if exposed to the Rh antigen. And that would be deadly when an Rh negative mother is pregnant with an Rh positive baby.

So how does this happen exactly? So during birth, Okay, this is our first exposure, so the birth of the first Rh-positive infant. Okay, so this first infant, totally fine.

Okay, during birth, the Rh-positive fetal erythrocytes are going to leak into the maternal blood. That's because we've broken off the embryonic chorion, and that normally isolates the fetal and maternal blood. But during birth, it's broken.

The maternal B cells would be activated by the Rh antigen that was present within the fetal or the baby. And that produces large amounts of anti-Rh antibodies. Now, in any next birth, now the Rh antibody within the mother's blood is elevated after that first exposure that happened.

So now the Rh antibodies are actually small enough to cross the embryonic chorion, and it can attack any fetal erythrocytes. So what I'd like you to do is take a second and fill in this chart, and that is one of your assignments. If you have any questions, please feel free to reach out to me.

I am here to answer them.

Transcript for:Understanding the Cardiovascular System

Transcript for:
Understanding the Cardiovascular System